Cognitive reactivity and vulnerability: empirical evaluation of construct activation and cognitive diatheses in unipolar depression

Cognitive vulnerability is a central concept in cognitive theories of unipolar depression. This idea suggests that negative cognitive factors emerge during stressful situations, and that this cognitive reactivity is critical for the onset, relapse, and recurrence of depression. The number of empirical investigations that model the diathesis-stress nature of cognitive reactivity has substantially increased within the last decade. This review examines this literature, with a focus on priming and longitudinal designs. Extant research supports the concept of cognitive vulnerability to depression among adults, and support is accruing for the validity of this concept among children. Research that examines direct links between cognitive vulnerability and depression onset, relapse, and recurrence and the attachment origins of cognitive vulnerability is also accruing, although at a slower pace.     

Geriatric depression and cognitive impairment

Cognitive impairment is common in geriatric depression, and depressed individuals with co-morbid cognitive impairment are at increased risk for a number of adverse medical, psychiatric and cognitive outcomes. This review focuses on clinical issues surrounding the co-occurrence of these two conditions within the context of current research. We (1) review the clinical criteria and prevalence of depression, as well as co-morbid cognitive impairment, (2) discuss factors associated with persistent cognitive impairment in depression, including dementia, and (3) review research relevant to the assessment and treatment of cognitive impairment and dementia in the context of depression. We conclude that current research on depression and cognition can inform clinical decisions that reduce the occurrence of adverse outcomes. Clinicians are encouraged to develop proactive approaches for treatment, which may include combinations of pharmacological and psychotherapeutic interventions.     

Remitted depression studies as tests of the cognitive vulnerability hypotheses of depression onset: a critique and conceptual analysis

Investigations of cognitive patterns among individuals who have recovered from a depressive episode (i.e., remitted depressives) have figured importantly in evaluations of the validity of the vulnerability hypotheses of the cognitive theories of depression. However, we suggest that remitted depression studies as typically conducted and interpreted are inadequate tests of the cognitive vulnerability hypotheses of depression onset for four reasons: (1) remitted depression studies are based on the erroneous assumption that cognitive vulnerability should be an immutable trait; (2) remitted depression studies use a logically "backward" participant selection strategy in which participants are selected on the basis of the "dependent" variable (depression) and then compared on the "independent" variable (cognitive vulnerability), which is likely to result in heterogeneity of cognitive vulnerability among both the remitted depressed as well as the nondepressed groups given the causal relations specified in the cognitive theories of depression; (3) many remitted depression studies have ignored the possible activating role of stress in the cognitive vulnerability-stress theories, particularly Beck's theory, and thus, may attempt to assess cognitive vulnerability at a time when it is not operative (i.e., priming hypothesis); and (4) remitted depression studies inappropriately use postmorbid participants to test causal hypotheses, and therefore, are ambiguous about whether negative cognitive styles observed in remitted depressed persons are vulnerabilities as opposed to consequences of depression (i.e., scar hypothesis). As a remedy, we advocate the use of a theory-guided behavioral high-risk strategy to more adequately test the cognitive vulnerability hypotheses of depression onset.     

Measuring cognitive vulnerability to depression: development and validation of the cognitive style questionnaire

The Cognitive Style Questionnaire (CSQ) measures the cognitive vulnerability factor featured in the hopelessness theory of depression. The CSQ has been used in over 30 published studies since its inception, yet detailed information about the psychometric and validity properties of this instrument has yet to be published. In this article, we describe the development of the CSQ and review reliability and validity evidence. Findings to date using college samples, indicate that the CSQ is a reliable measure of cognitive vulnerability with a high degree of construct validity.     

A cognitive vulnerability-stress perspective on bipolar spectrum disorders in a normative adolescent brain, cognitive, and emotional development context

Why is adolescence an "age of risk" for onset of bipolar spectrum disorders? We discuss three clinical phenomena of bipolar disorder associated with adolescence (adolescent age of onset, gender differences, and specific symptom presentation) that provide the point of departure for this article. We present the cognitive vulnerability-transactional stress model of unipolar depression, evidence for this model, and its extension to bipolar spectrum disorders. Next, we review evidence that life events, cognitive vulnerability, the cognitive vulnerability-stress combination, and certain developmental experiences (poor parenting and maltreatment) featured in the cognitive vulnerability-stress model play a role in the onset and course of bipolar disorders. We then discuss how an application of the cognitive vulnerability-stress model can explain the adolescent age of onset, gender differences, and adolescent phenomenology of bipolar disorder. Finally, we further elaborate the cognitive vulnerability-stress model by embedding it in the contexts of normative adolescent cognitive (executive functioning) and brain development, normative adolescent development of the stress-emotion system, and genetic vulnerability. We suggest that increased brain maturation and accompanying increases in executive functioning along with augmented neural and behavioral stress-sensitivity during adolescence combine with the cognitive vulnerability-stress model to explain the high-risk period for onset of bipolar disorder, gender differences, and unique features of symptom presentation during adolescence.     

The origins of cognitive vulnerability in early childhood: mechanisms linking early attachment to later depression

This paper examines the theory and research linking attachment relationships to cognitive vulnerability to depression and assesses evidence that early attachment experiences contribute to the development of these cognitive processes. Most research in this area has involved adult participants using self-report measures of both attachment and depressive vulnerabilities and thus cannot convincingly speak to the existence of such a developmental pathway. Several studies, however, have followed individuals from infancy and examined the emergence of self-esteem and responses to failure throughout childhood and adolescence. These studies suggest that early experiences in non-secure attachment relationships place an individual at-risk for developing a cognitive framework that increases their vulnerability to depression following stressful life events. The paper concludes with a discussion of how future research might best explore specific mechanisms through which distinct attachment relationships may lead to divergent developmental pathways sharing the common outcome of cognitive processes that place individuals at risk for depression.     

The combined cognitive bias hypothesis in depression

Drawing from substantial evidence demonstrating cognitive biases in depression at various stages of information processing (i.e., attention, interpretation, memory, cognitive control), we argue for an approach that considers the interplay among these processes. This paper attempts to apply the combined cognitive bias hypothesis (Hirsch, Clark, & Mathews, 2006) to depression research and reviews competing theoretical frameworks that have guided research in this area. We draw on current findings from behavioral studies on the interplay between depression-related processing biases. These data indicate that various cognitive biases are associated. However, it is not clear whether single or multiple biases are most predictive of depressive symptoms. We conclude this article with theoretical and clinical implications of the current state of research in this field and propose a number of ways in which research on the combined cognitive bias hypothesis can be advanced.     

A longitudinal investigation of information processing and cognitive organization in clinical depression: stability of schematic interconnectedness.

This study longitudinally investigated information processing and cognitive organization in clinical depression. The main hypothesis was that individuals whose depression had remitted would show a significant cognitive shift on information processing (e.g., deactivation of negative processing) but not on cognitive organizational tasks, Forty-five individuals with clinical depression completed 2 information processing and 2 cognitive organizational tasks at initial assessment. At 6-month follow-up, the sample (23 remitted, 22 stable depressed) was readministered the tasks. As expected, information processing shifted significantly in individuals who had improved symptomatically, whereas negative cognitive organizational indices remained stable. The implications of these results are discussed as they pertain to the cognitive vulnerability, maintenance, treatment, and recurrence of depression. Directions for future research are suggested.     

Comparative data on child and adolescent cognitive measures associated with depression

As a way to better understand the effects of treatment for depression, comparative data on measures of cognition have been compiled previously for adults. Such data should be able to aid the evaluation of cognition and cognitive change, and may provide valuable information for clinicians and researchers alike. In this article, analogous comparative data on cognitive measures associated with depression in children and adolescents are presented. The reviewed instruments assess cognitive errors, attributional style, dysfunctional attitudes, hopelessness, negative self-statements, and Beck's negative cognitive triad. As with adults, these data may have implications for enhancing understanding of empirically supported treatments for children and adolescents, may be useful in vulnerability research, and may be useful to clinicians seeking to develop treatment strategies and to gauge treatment effectiveness.     

Amygdala hyperactivation and prefrontal hypoactivation in subjects with cognitive vulnerability to depression

The hopelessness theory (HT) of depression is a diathesis-stress theory which construes cognitive vulnerability (CV) to depression. Neuroimaging studies examining depression have implicated the amygdala as an important potential locus of dysfunction in the processing of salient threatening stimuli. However, little is known about neural activation in the brain of subjects with CV to depression. Medication-free major depressive disorder (MDD) subjects (N=29), never depressed subjects with CV (N=26), and demographically matched never depressed healthy control (HC) subjects (N=31) were scanned using functional magnetic resonance imaging (fMRI) while performing an emotional matching task. The MDD subjects showed elevated left amygdala responses and reduced left dorsolateral prefrontal cortex (dlPFC) activation levels relative to HC subjects. Similarly, CV subjects had greater activity in the amygdala bilaterally and lesser activation in the dlPFC bilaterally, relative to HC subjects. The present findings raise the possibility that cognitive vulnerability to depression might be characterized by hypoactivation of the prefrontal cortex and hyperactivation of the amygdala in response to emotional stimuli; our observations might provide a potential interpretation to explain the abnormalities in neural networks mediating cognitive modulation of emotions in individuals with cognitive vulnerability to depression.     

Voxel-based morphometric gray matter correlates of daytime sleepiness

We theorized the cognitive vulnerability factor featured in hopelessness theory [2] to be a novel endophenotype for depression. We investigated two possible genetic contributors to individual differences in cognitive vulnerability (and, in turn, depression): the BDNF gene and the COMT gene. Results showed that individuals (n = 95) with the BDNF Val⁶⁶ genotype had significantly greater levels of cognitive vulnerability than individuals with a BDNF Met⁶⁶ genotype. In addition, among individuals with high levels of cognitive vulnerability, those with the Val⁶⁶ genotype were significantly more likely than participants with a Met⁶⁶ genotype to experience increases in depressive symptoms when faced with increased stress. The COMT gene was not associated with cognitive vulnerability or risk for depression. Results support the use of the cognitive vulnerability factor featured in hopelessness theory as an endophenotype associated with depression as well as the role of the BDNF gene in a cognitive subtype of depression.     

Developmental origins of cognitive vulnerabilities to depression: review of processes contributing to stability and change across time

Cognitive theories of depression have been shown to be potent predictors of future increases in depressive symptoms and disorder in children, adolescents, and adults. This article focuses on potential developmental origins of the main cognitive vulnerabilities, including dysfunctional attitudes, negative cognitive style, and rumination. We selectively review processes and factors that have been hypothesized to contribute to the emergence and stabilization of these cognitive risk factors. This review focuses on genetic factors, temperament, parents and peers as salient interpersonal influences, and stressful life events. We end with suggestions for future theory development and research. In particular, we emphasize the need for additional conceptual and empirical work integrating these disparate processes together into a coherent, developmental psychopathological model, and we highlight the coexistence of both stability and change in the development of cognitive vulnerabilities to depression across the lifespan. © 2009 Wiley Periodicals, Inc. J Clin Psychol 65:1–12, 2009.     

The psychosocial context of bipolar disorder: environmental, cognitive, and developmental risk factors

In this article, we review empirical research on the role of individuals' current environmental contexts, cognitive styles, and developmental histories as risk factors for the onset, course, and expression of bipolar spectrum disorders. Our review is focused on the following over arching question: Do psychosocial factors truly contribute risk to the onset, course, or expression of bipolar disorders? As a secondary issue, we also address whether the psychosocial risks for bipolar disorders are similar to those for unipolar depression. We begin by discussing the methodological requirements for demonstrating a psychosocial risk factor and the challenges posed by bipolar spectrum disorders for psychosocial risk research. Next, we review the extant studies on the role of recent life events and supportive and non-supportive social interactions (current environment) in bipolar disorders, as well as psychosocial treatments designed to remediate these current environmental factors. We then review the role of cognitive styles featured as vulnerabilities in theories of unipolar depression as risk factors for bipolar disorder alone and in combination with life events, including studies of cognitive-behavioral therapies for bipolar disorder. Finally, we review studies of parenting and maltreatment histories in bipolar disorders. We conclude with an assessment of the state of the psychosocial risk factors literature in bipolar disorder with regard to our guiding questions.     

Family processes in the development of youth depression: Translating the evidence to treatment

There is strong evidence that family factors play a role in the development, maintenance and course of youth depression. However, to date few clinical trials of psychotherapy for youth depression employ family therapy interventions or target the known family risk factors. This is surprising given recent meta-analytic findings showing only modest effect sizes for psychotherapy for youth depression, and that cognitive therapies do not outperform non-cognitive therapies. The aim of this review is to 1) use a developmental systems approach to review empirical evidence on family risk factors for youth depression to identify potential targets for treatment, 2) examine the extent to which these family risk factors have been targeted in clinical trials for youth depression, and 3) provide a road map for the development of empirically validated family-based interventions for youth depression.     

Emotion socialization within the family environment and adolescent depression

This review evaluates research addressing the association between parent-child emotional interactions and the development and maintenance of depression in adolescence, with a focus on studies using observational research methods that assess parental responses to children and adolescents' emotional displays. We argue that parental socialization behaviors in response to different emotions expressed by youths may have distinct associations with depressive outcomes. In particular, parental behaviors that reinforce depressive behavior, reciprocate aggression, and fail to positively reinforce positive behavior have each been associated with youth depression. This review identifies a need for more observational research, including prospective, longitudinal studies, to better understand these behaviors, elucidate the directionality of influence between parental socialization behaviors and youth depression, and more clearly identify protective parental socialization behaviors. However, the use of existing findings to inform family-based interventions may improve prevention and treatment efforts directed at youth depression.     

A review on cognitive impairments in depressive and anxiety disorders with a focus on young adults

BACKGROUND: There is growing evidence for cognitive dysfunction in depressive and anxiety disorders. Nevertheless, the neuropsychological profile of young adult patients has not received much systematic investigation. The following paper reviews the existing literature on cognitive impairments in depressive and anxiety disorders particularly among young adults. Additionally, the focus of young adult age group and the effect of confounding variables on study results are discussed. METHODS: Electronic database searches were conducted to identify research articles focusing on cognitive impairments in depressive or anxiety disorders among young adults published in English during years 1990-2006. RESULTS: Cognitive impairments are common in young adults with major depression and anxiety disorders, although their nature remains partly unclear. Accordingly, executive dysfunction is evident in major depression, but other more specific deficits appear to depend essentially on disorder characteristics. The profile of cognitive dysfunction seems to depend on anxiety disorder subtype, but at least obsessive-compulsive disorder is associated with deficits in executive functioning and visual memory. The conflicting results may be explained by heterogeneity within study participants, such as illness status, comorbid mental disorders, and medication, and other methodological issues, including inadequate matching of study groups and varying testing procedures. LIMITATIONS: The study is a comprehensive review, but not a formal meta-analysis, due to methodological heterogeneity. CONCLUSIONS: Cognitive impairments are common in major depression and anxiety disorders. However, more research is needed to confirm and widen these findings, and to expand the knowledge into clinical practice. Controlling of confounding variables in future studies is highly recommended.     

Autobiographical memory predicts cognitive but not somatic change in sleep apnea patients vulnerable for affective disorder

BACKGROUND: Autobiographical memory style (AM) can serve as a marker for determining susceptibility for depression. Currently and formerly depressed persons show reduced specific memory for autobiographical events. AM also has proven to be a reliable predictor for the remissive course of depression. Recently the issue arose as to whether this predictive power depends on particular dimensions of depression (cognitive, somatic). METHODS: To replicate the predictability in vulnerable patients, we tested two groups of obstructive sleep apnea patients (OSAS) before and 2 months after initiation of nasal continuous positive airway pressure therapy (nCPAP). One group had a history of major depression (vulnerable persons; VUL), and the other group did not (NON-VUL). Sensitivity of AM on the dimensions of depression was assessed through two published versions of the cognitive and somatic subscales of the Beck Depression Inventory (BDI). RESULTS: There was a significant interaction of Group by AM recall after presentation of positively valenced cues (AMpos) on the cognitive but not on the somatic dimension of the BDI. Only in the VUL did AMpos predict recovery. LIMITATIONS: Generalizability to other patient populations awaits further research. Reliability of the vulnerability assessment prior to the OSAS onset was not established. CONCLUSIONS: First, our findings further support the trait assumption of AM. Second, the AM methodology suggests sensitivity to only the cognitive dimensions of depression.     

Cognitive vulnerability to depression: a dual process model

Dual process models offer powerful accounts of cognitive phenomena in social and personality psychology but they have not been widely adapted to clinical phenomena. This review presents a dual process model of cognitive vulnerability to unipolar depression. According to dual process theories, humans possess two modes of information processing. An associative mode involves quick, effortless processing that rests on well-learned associations. A reflective mode involves slow, effortful processing that rests on symbolic rule-based inferences. Whereas the associative mode occurs automatically, the reflective mode operates when expectancies are violated and sufficient cognitive resources are available to respond. A cognitive vulnerability to depression is observed when negatively biased associative processing is uncorrected by reflective processing. The circumstances when this is likely to occur are reviewed. New insights and implications for assessment, etiology, and treatment of cognitive vulnerability to depression are discussed.     

Physiological response and childhood anxiety: association with symptoms of anxiety disorders and cognitive bias.

This study examined the physiological response (skin conductance and heart rate [HR]) of youth exposed to a mildly phobic stimulus (video of a large dog) and its relation to child- and parent-reported anxiety symptoms and cognitive bias in a community-recruited sample of youth (n = 49). The results of this study indicated that HR and skin-conductance response were associated with youth report but not parent report of their child's symptoms of anxiety disorders and that HR response was more strongly associated with anxiety symptoms than skin-conductance response. Physiological response was uniquely associated with youth-reported symptoms of anxiety rather than youth-reported depression. Finally, HR response interacted with cognitive bias in predicting childhood anxiety disorder symptoms in a manner consistent with theories of the etiology of anxiety disorders.     

Comparison of cognitive impairment associated with major depression following stroke versus traumatic brain injury

Several studies have reported an association between cognitive impairment and major depression following stroke but failed to find a similar association among patients with traumatic brain injury (TBI). This study examined the hypothesis that age differences between stroke and TBI patients would account for the differences in the effect of major depression on cognitive function. We examined subjects' cognitive function using the Mini-Mental State Examination and compared findings among patients with stroke or TBI. Results indicated that stroke patients with major depression (N = 73) were significantly older and more cognitively impaired than similar TBI patients (N = 35), even after matching patients for lesion volume and years of education. After matching for age, however, there was no association of major depression with cognitive impairment in this relatively young stroke population. These findings support the hypothesis that age, presumably related to physiological response to brain injury, accounts for differences in the effect of major depression on cognitive function between stroke and TBI patients.